Herpesvirus infection accelerates atherosclerosis in the apolipoprotein E-deficient mouse.
779 - 785.
BACKGROUND: Human herpesviruses have been implicated but not proven to be involved in the etiology of atherosclerosis. To determine whether there is a causal relationship, the effect of herpesvirus infection on the development of atherosclerosis was assessed in the apolipoprotein E- deficient (apoE-/-) mouse. METHODS AND RESULTS: In the present study, 3- to 4-week-old apoE-/- mice were infected with murine gamma-herpesvirus- 68 (MHV-68). Atheroma formation was accelerated over a 24-week period in infected apoE-/- mice compared with control uninfected apoE-/- mice. Acceleration of atherosclerosis was reduced by antiviral drug administration. Histological analysis of the atheromatous plaques showed no difference between lesions of infected and control mice. Viral mRNA was present in the aortas of infected mice before lesion development on day 5 after infection. This suggests that the virus may initiate endothelial injury, which is believed to be an early event in the development of atherosclerosis. Therefore, the virus may play a direct role in atherosclerosis rather than be an "innocent bystander." CONCLUSIONS: These data demonstrate that a gamma-herpesvirus can accelerate atherosclerosis in the apoE-/- mouse. This study provides the first report of a murine model in which to study the causative role of herpesvirus infection in the development of atherosclerosis
|Title:||Herpesvirus infection accelerates atherosclerosis in the apolipoprotein E-deficient mouse|
|Additional information:||UI - 20402318 LA - eng RN - 0 (Antiviral Agents) RN - 0 (Apolipoproteins E) RN - 0 (RNA, Messenger) RN - 0 (RNA, Viral) RN - 57-88-5 (Cholesterol) PT - Journal Article DA - 20000905 IS - 1524-4539 SB - AIM SB - IM CY - UNITED STATES JC - DAW|
|Keywords:||Infection, mouse, analysis, Animal, Antibody Formation, Antiviral Agents, Aorta, Apolipoproteins, Apolipoproteins E, Arteriosclerosis, Blood, Cholesterol, complications, control, deficiency, development, difference, drug therapy, Endothelial, Endothelium, Vascular, etiology, formation, genetics, Herpesviridae, Herpesviridae Infections, Infection, injuries, injury, isolation & purification, May, metabolism, Methods, mice, Mice, Knockout, model, mRNA, murine, pathology, Plaque, Research, Rna, RNA, Messenger, Viral, STATE, STATES, Support, Non-U.S.Gov't, therapeutic use, Time Factors, UK, United States, virology, VIRUS|
|UCL classification:||UCL > School of Life and Medical Sciences > Faculty of Medical Sciences > Medicine (Division of)|
Archive Staff Only